penis enlargement pump in pakistan use for size up penis but Penile elongation surgery is less commonly performed in the public sector, but involves a collaborative approach between urology and plastic surgery. Congenital and acquired micropenis are the classic surgical indications for penile elongation surgery. The goal of intervention in these patients is to restore a functional penis size in order to allow normal standing micturition, enable satisfying sexual intercourse and improve patient quality of life. Many men seeking elongation actually have normal length penises, but perceive themselves to be small, a psychological condition termed ‘penile dysmorphophobia’. This paper will review the anatomy and embryology of congenital micropenis and discuss both conservative and surgical management options for men seeking penile elongation therapy.
To fully understand limitations of small penis size and the surgical correction possibilities, we must review the relevant basic penile anatomy. The penis is composed of three large cylinders—two corpora cavernosa dorsally, which contain the erectile tissue, and the corpus spongiosum which constitutes the urethra. The main components of the penis are surrounded by areolar tissue and peripherally encased with skin. Each layer of the penis plays a significant role in the function and dynamics of the penis during sexual activity and voiding (1).
Skin plays an important role in protecting the penile tissues from trauma during intercourse and as a barrier from bacterial infection. If infection or trauma do occur, the skin can impair intracavernosal functioning and result in a contained abscess or hematoma formation, respectively. The skin is firmly attached to the glans and only loosely attached to the shaft, allowing for mobility during intercourse. Deep to the skin lies the superficial (dartos) and deep (Bucks’) fascia, which supply additional structural support (2). At the base of the penis, the dartos fascia combines with smooth muscle fibres and creates a well-defined penoscrotal angle between the scrotal wall and the skin. The deep fascia adheres to the tunica albuginea (1).
The base of the penis is firmly attached to the pubic rami by penile ligaments composed of connective tissue. The ligaments arise from the external oblique aponeurosis and are fixed to the symphysis pubis. The suspensory ligament arises from the linea alba and provides dorsal support and stabilization of an erection by attaching midline to the penile root (2). This ligament also helps cover the neurovascular bundle of the penis and protects it during repetitive sexual trauma. The ligament of Luschka or fungiform ligament consist of dartos fibers and extends from the abdominal Scarpa’s fascia onto the penile shaft. The fungiform ligament attaches to the pubis and fans laterally and ventrally to the encircle the entire penile root, acting like a sling for support (1).
During embryologic development, gender remains indifferent until approximately seventh week of gestation. From the eighth week onward, male and female developmental pathways diverge. In males, maternal chorionic gonadotropins from the placenta stimulate growth and development of the testicular Leydig cells, which eventually produce their own testosterone for further development (3). The development of the external genitalia in males is dependent on the conversion of testosterone to the active component dihydrotestosterone (DHT). Testosterone is converted to DHT locally by 5 α-reductase and then directly acts on androgen receptors to initiate cell signaling pathways (3,4).
The genital tubercle enlarges to form both the shaft and glans of the penis. The urogenital folds fuse along the midline to become the penile urethra and the glans invaginates to create the glandular urethra. The labioscrotal folds fuse to create the scrotum. Complete penile differentiation should be complete by the end of the first trimester. Penile length and size increase during development in proportion to other fetal development (5). The average penile length increases by a mean of approximately 2 cm between 14 weeks and term. Penile elongation in utero is complete by androgens produced by the fetus. After the first trimester, the fetus depends on his own hypothalamic-pituitary axis for gonadotropin production. Any abnormality resulting in hypogonadism in utero can result in an underdeveloped penis, and therefore congenital or ‘true’ micropenis (5,6).
After normal development, there is an LH surge at birth which stimulates an increase in testosterone production and penile growth. This surge only lasts about 12 h and subsequently hormone levels drop quite low. Slowly, gonadotropin and androgen levels begin to rise and peak again. This rise in levels lasts for approximately 6 months and allows for continued penile growth (7). Ongoing penile growth occurs throughout development, without the need for surges, but rather as a result of normal growth. At puberty, the HPG axis gets activated and stimulates testicular testosterone production, which subsequently leads to further penile growth into adulthood (7,8)
Accurate measurement of penile length is important for both clinical and academic purposes. For this reason, a standard practice for measurement has been defined to maintain consistency. Rather than measuring a flaccid penis, which offers limited clinical significance, stretched penile length (SPL) measurement is considered best practice for adult men as it most closely replicates normal erect penile length (9). SPL is the maximum length of the penis while stretched, measured from the base of the penis, under the pubic symphysis to the tip of the glans and is thought to approximate erect penile length within 10% (10). For accurate clinical assessment, SPL needs to be measured by a clinician. Studies have demonstrated that men who are satisfied with their penile length overestimate their size, whereas men who are dissatisfied consistently underestimate (11).
True micropenis is defined as a normally formed penis that has an SPL that falls below two standard deviations of normal for a patient’s age and race (12). Wiygul outlined the mean SPL in children as well as the diagnostic length for micropenis at each age (13). Normal values for preterm infants born between the 24th and 36th week of gestation can be calculated using the formula: (0.16 × weeks of gestation) – 2.27 (14).
As mentioned, micropenis develops as a result of a central or local hormonal imbalance during fetal development. True micropenis is a congenital anomaly and is different from acquired penile length abnormalities such as buried penis or trapped penis. Based on the etiology of the hormonal dysfunction, micropenis can be divided into three broad categories: hypogonadotropic hypogonadism, hypergonadotropic hypogonadism, and idiopathic. Other, less common causes of micropenis have been documented and are listed in Table 1. Disorders of sexual differentiation may present with micropenis, although hypospadias is more common (13). The coexistence of micropenis and hypospadias is termed “microphallus” (1).
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